The nematode Caenorhabditis elegans has been used as a model for the genetic studies of aging. Mutations in the Clock-1 (clk-1) gene of C. elegans result in slowed development and rhythmic behaviors, and an extended life span. The C. elegans clk-1 gene is a homologue of COQ7, a gene in Saccharomyces cerevisiae required for the biosynthesis of ubiquinone (coenzyme Q). The nematode, rat and human homologs of clk-1/COQ7 all function to restore coenzyme Q biosynthesis in the yeast coq7 null mutant. Given the functional conservation of yeast rat, human and C. elegans CLK-1/Coq7 polypeptides, it is crucial to test whether changes in the level of coenzyme Q may be responsible for the slowed development, behavior and rate of aging in the nematode model. The studies proposed are designed to answer the following questions: (1) Do mutations in the clk-1 gene have effects on the level of coenzyme Q in C. elegans? (2) Are rates of development, adult behaviors, or life span affected when the C. elegans clk-1 mutants are grown on E. coli lacking coenzyme Q? and (3) What is the phenotype of a C. elegans coq null mutant? In order to examine these questions, the levels of coenzyme Q, the developmental timing, and the life span of the clk-1 mutant and wild type strains will be determined as a function of the type E. coli food source; both coenzyme Q-replete and coenzyme Q- deficient E. coli strains will be used. These studies will determine the effect of the clk-1 mutations on the biosynthesis of coenzyme Q in the nematode system; a model that is ideal for evaluating the relationship between coenzyme Q and aging. It is also likely that these studies will indicate whether C. elegans can provide a metazoan model uniquely suited to address questions regarding coenzyme Q uptake, metabolism and redistribution.